| Project/Area Number |
15K10249
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular surgery
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| Research Institution | Kurume University |
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Principal Investigator |
OHNO Satoko 久留米大学, 医学部, 助教 (80569418)
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| Co-Investigator(Kenkyū-buntansha) |
青木 浩樹 久留米大学, 付置研究所, 教授 (60322244)
田中 啓之 久留米大学, 医学部, 教授 (70197466)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 大動脈解離 / マクロファージ / 平滑筋 / サイトカイン / 増殖応答 / 炎症 / 機能分化 / 組織修復 / 炎症応答 / 細胞増殖 |
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| Outline of Final Research Achievements |
We examined the hypothesis that macrophage Stat3 promotes the aortic dissection (AD) through the differentiation of macrophage and vascular smooth muscle cell (VSMC) . We found that macrophage-specific Socs3-KO (mSocs3-KO), in which Stat3 is enhanced specifically in macrophages, developed AD following minor aortic injury by aortic stress. In mSocs3-KO, macrophages predominantly differentiated to proinflammatory phenotype, resulting in the aortic inflammation enhancement. In the wild type, VSMC showed increase in tissue repair function upon aortic stress. In contrast, the tissue reparative phenotype of VSMC was suppressed in mSocs3-KO. As the mechanism of the dysregulation of VSMC, Ink4a/Arf, an inhibitor of proliferation which is also well known as the regulator of tissue repair, was highly expressed at minor injury in mSocs3-KO.
These results indicated that development of AD is driven by the imbalance of destruction and repair during the inflammation following the aortic stress.
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